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Height and width of the scala vestibuli were measured on resin casts at seven different places, beginning at the round window up to 1 3/4 turns of the cochlea. These figures do not decrease continuously but are augmented at certain places. The sectional areas of both scales show the same result according to the transient increases of height and width.
(1) The loss of hair cells after pure tone exposure at the critical level of intensity shows an exact correlation to the frequency, the time of sound exposure, and time of recovery as regards the quality and quantity. (2) The total extent of the damage of sensory cells has to be estimated higher than the hair-cell loss as observed under the light microscope. Although an improvement of the function of the organ of Corti was determined electrophysiologically from the 5th to the 10th day of recovery, the hair-cell degeneration was progredient during this period. (3) The hair-cell damage is apically more strongly marked from the area of damage than basically. (4) Depending on the experimental conditions there are considerable degenerative alterations in the nerve fibres and in the connective apparatus of the organ of Corti besides hair-cell losses and damages.
The influence of simple opening of the round window (RW) membrane and the effect of aspiration of perilymph on the electrophysiological characteristics of the cochlea was tested in guinea pigs by measurement of the compound action potentials. We found that perforations of the RW membrane failed to lead to either short-term or long-term damage in cochlear function. There was only a slight spontaneous escape of perilymph but without measurable functional loss. Additional aspiration of perilymph led to entry of air into the basal turn and to an immediate loss of function of the cochlea. This regressed within 4 weeks in the middle- and low-frequency ranges. Measurable long-term damage persisted only in the high-frequency ranges. We attribute contradictory results of other authors to methodological errors which we avoided by a specific selection of healthy animals and the development of standardized operation, recording and measurement procedures.
We reported that apoptosis occurred in the guinea pig vestibular hair cells after chronic aminoglycoside treatments. In the present study, we used in situ nick-end labeling to determine whether apoptosis was also induced by the acute effects of aminoglycosides in guinea pig ampullar cristae. In addition, we evaluated the effect of zinc supplements upon these ototoxic treatments. After a local application of streptomycin directly to the round window, we found labeled bodies in the vestibular hair cells. The zinc supplement increased the number of labeled bodies resulting in severe hair cell loss. These findings indicate that the acute effects of aminoglycosides also induce apoptosis of the vestibular hair cells, and that zinc enhances aminoglycoside ototoxicity. Consequently, we propose that an interaction with ion channels may play a key mechanism in the processes of apoptosis affecting the vestibular hair cells.
Dimensions of the scala tympani were measured at eight different places of 1 3/4 turns of the cochlea, beginning at the round window. Height and width of the scala tympani do not decrease continuously but show enlargements in some places. The diameter of two types of cochlear implants were compared with the mean heights of the scala tympani. The data provide an anatomical basis for the development of cochlear prosthesis, which could be inserted for a longer distance as accomplished hitherto.
In guinea pigs the tympanic perilymph of the basal turn was marked with fluorescing rhodamine. In the first series one drop of a 2% solution of the dye was applied onto the round window membrane. Since the perilymphatic space was not opened, the physiologic state of the communicating fluids perilymph and CSF was maintained. The dye appeared within 3-5 min via cochlear aqueduct in the subarachnoidal space. In the dead animal the speed of distribution was significantly less. This most probably indicates a weak physiologic flow of the perilymph through the aqueduct to the subarachnoidal space in living animals. In the second series, 2 ng of lyophilized rhodamine was instilled directly into the tympanic perilymph near the round window. Though hardly any additional volume was brought into the perilymph, the distribution of the dye was distinctly greater as a sign of the considerable sensitivity of the fluid system, even by the slightest manipulation.
BACKGROUND: Intraoperative measurements of local intracapillary hemoglobin oxygenation of the human cochlea via the round window membrane have been shown to be possible using the Erlangen microlight-guided spectrophotometer. The aim of the present study was to develop a new microlight guide suitable for measurements in the round window niche and to evaluate electrophysiologically the possible impact of the procedure on the cochlea. METHODS: Measurements were made for wavelengths of 450 to 900 nm at a total power of 5.3 mW. The exit diameter of the light guide was 200 microns and the angle used was 20 degrees. The recording depth was about 250 microns. The atraumatic character of the spectrophotometry was demonstrated by monitoring the compound action potential (CAP) threshold tuning curve from 1 to 34 kHz in ketanest-anesthetized guinea pigs. RESULTS: CAP thresholds remained constant (0.3 +/- 3.9 dB SPL) during 3 to 30 min of exposure to the light. CONCLUSIONS: These results suggest that the spectrophotometry may be useful as a new technique for intraoperative monitoring of intracapillary hemoglobin without causing physiological deterioration of the cochlea.
Microinjection through the round window membrane has been found to represent a method for vector delivery in intracochlear gene transfer in animal models but breaches the round window membrane, making it necessary to evaluate animals for possible postinjection hearing loss. In the present study healthy guinea pigs were evaluated for their baseline click auditory brainstem response (ABR) thresholds. Each animal was then injected with saline via the round window membrane. After 1 week auditory function was evaluated by click ABR. Animals with increased ABR thresholds were retested at 4 weeks. Animals with 1-week postoperative ABRs similar to baseline were not retested. Results showed that postoperative ABR thresholds in five animals (71%) remained unchanged from baseline, while two animals had increases of 20-25 dB in ABRs after 1 week but recovered baseline ABRs after 4 weeks. The mean baseline ABR threshold was 25.7 dB and was 27.9 dB after 1 week after injection. The difference between preoperative and 1-week postoperative averages was not significant (P = 0.707). In this preliminary study saline microinjection through the round window membrane did not cause permanent hearing loss in the guinea pigs tested, and any damage caused by microinjection appeared to be reversible.
Prostaglandins (PGs) such as PGE2 and PGI2 are vasodilators, and leukotrienes (LTs) such as LTB4 and LTC4 are vasoconstrictors. Our previous studies have shown that salicylate ototoxicity is associated with decreased levels of PGs and increased levels of LTs. We hypothesized that vasodilating PGs increase cochlear blood flow and vasoconstricting LTs decrease cochlear blood flow. PGE2, Iloprost (a PGI2 analog), LTB4, and LTC4 were applied to the round window membranes of chinchillas and cochlear blood flow was measured with a laser Doppler flowmeter. PGE2 increased cochlear blood flow, while LTC4 decreased cochlear blood flow. This findings show that vasodilating PGs may have therapeutic implications for sensorineural hearing loss and/or vertigo by increasing cochlear blood flow. Vasoconstricting LTs may cause hearing loss by decreasing cochlear blood flow.
Glutamate excitotoxicity is implicated in both the genesis of neural injury and noise-induced hearing loss (NIHL). Acoustic overstimulation may result in excessive synaptic glutamate, resulting in excessive binding to post-synaptic receptors and the initiation of a destructive cascade of cellular events, thus leading to neuronal degeneration and NIHL. The purpose of this study was to determine whether this apparent excitotoxicity can be attenuated by kynurenic acid (KYNA), a broad-spectrum glutamate receptor antagonist, and protect against noise-induced temporary threshold shifts (TTS). Guinea pigs were randomly assigned to three separate groups. Base-line compound action potentials (CAP) thresholds and cochlear microphonics (CM) were recorded. Group I was treated with physiologic saline as a vehicle control applied to the round window membrane that was followed by 110 dB SPL wide-band noise for 90 min. Group II received 5 mM KYNA followed by noise exposure, and group III received 5 mM KYNA alone without noise exposure. Post-drug and noise levels of CAP thresholds and CM were then obtained. Noise exposure in the control group caused a significant temporary threshold shift (TTS) of 30-40 dB across the frequencies tested (from 3 kHz to 18 kHz). Animals that received 5 mM KYNA prior to noise exposure (group II) showed statistically significant protection against noise-induced damage and demonstrated a minimal TTS ranging between 5 and 10 dB at the same frequencies. Animals in group III receiving KYNA without noise exposure showed no change in thresholds. Additionally, cochlear microphonics showed no considerable difference in threshold shifts when controls were compared to KYNA-treated animals. These results show that antagonizing glutamate receptors can attenuate noise-induced TTS, suggesting that glutamate excitotoxicity may play a role in acoustic trauma.
Using a laser velocimeter, responses to tones were measured at a basilar membrane site located about 1.2 mm from the extreme basal end of the gerbil cochlea. In two exceptional cochleae in which function was only moderately disrupted by surgical preparations, basilar membrane responses had characteristic frequencies (CFs) of 34-37 kHz and exhibited a CF-specific compressive nonlinearity: Sensitivity near the CF decreased systematically and the response peaks shifted toward lower frequencies with increasing stimulus level. Response phases also changed with increases in stimulus level, exhibiting small relative lags and leads at frequencies just lower and higher than CF, respectively. Basilar membrane responses to low-level CF tones exceeded the magnitude of stapes vibrations by 54-56 dB. Response phases led stapes vibrations by about 90 degrees at low stimulus frequencies; at higher frequencies, basilar membrane responses increasingly lagged stapes vibration, accumulating 1.5 periods of phase lag at CF. Postmortem, nonlinearities were abolished and responses peaked at approximately 0.5 octave below CF, with phases which lagged and led in vivo responses at frequencies lower and higher than CF, respectively. In conclusion, basilar membrane responses near the round window of the gerbil cochlea closely resemble those for other basal cochlear sites in gerbil and other species.
The physiological and morphological changes resulting from acute and chronic infusion of ouabain onto the intact round-window (RW) membrane were examined in the gerbil cochlea. Osmotic pumps fitted with cannulas allowed chronic (0.5-8 days) infusions of ouabain. Acute and short-term applications of ouabain (1-24 h) induced an increase in auditory-nerve compound action potential (CAP) thresholds at high frequencies with lower frequencies unaffected. The resulting threshold shifts were basically all (no response) or none (normal thresholds), with a sharp demarcation between high and low frequencies. Survival times of 2 days or greater after ouabain exposure resulted in complete auditory neuropathy with no CAP response present at any frequency. Distortion product otoacoustic emissions (DPOAEs) and the endocochlear potential (EP) were largely unaffected by the ouabain indicating normal function of the outer hair cells (OHC) and stria vascularis. One to 3 days after short-term applications, apoptosis was evident among the spiral ganglion neurons assessed both morphologically and with TdT-mediated dUTP-biotin nick end labeling (TUNEL). With 4-8 day survival times, most spiral ganglion cells were absent; however, a few cell bodies remained intact in many ganglia profiles. These surviving neurons had many of the characteristics of type II afferents. Our working hypothesis is that the ouabain induces a spreading depression among the type I ganglion cells by blocking the Na,K-ATPase pump. Because of the constant spike activity of these cells, the ouabain rapidly alters potassium concentrations within ([K+]i) and external to ([K+]o) the ganglion cells, thereby initiating an apoptotic cascade.
Compound auditory nerve action potentials (APs) and cochlear microphonics (CMs) were recorded from the round-window of kittens aged 3-9 weeks and of adult cats. Animals were anaesthetized and pure tone stimuli were delivered via calibrated, sealed, transducer systems. AP and CM amplitude and AP latency were measured over a wide range of stimulus intensities (up to 80 dB SPL) and at 5 octave-interval stimulus frequencies (1-16 kHZ). At low stimulus intensity levels, AP amplitude had attained adult levels to low and high frequency stimuli by 6 1/2 weeks of age and to mid-frequency stimuli by 9 weeks. As stimulus intensity levels were increased, the kitten input-output functions diverged progressively from those of the adults. At these higher intensity levels, AP amplitude maturation in even the 9 week animals was incomplete. AP latencies to stimuli of all frequencies shortened between the third and fourth weeks but remained stable thereafter. CM amplitude also reached maturity by the fourth week. These findings suggest that the development of AP after the fourth week consists of an increase in the synchrony of auditory nerve fibre responses, since both the fine structure of the cochlea and the responses of single nerve fibres are known to be mature by the end of the first postnatal month.
The gross responses from the cochlea (round window) and two nuclei of the ascending auditory pathway of the rat in response to tone and noise bursts (compound action potentials) were compared with those recorded in response to continuous tones and noise that was amplitude modulated with pseudorandom noise. The cross-correlation function between: (1) the averaged response to the sounds that were amplitude modulated with the pseudorandom noise, and (2) one period of the pseudorandom noise, were obtained. The compound action potentials and the cross-correlation functions both had a series of peaks. The two functions had a similar morphology. The latency of the peaks in the cross-correlation showed less dependence on sound intensity than did the latency of the peaks in the compound action potentials.
Frequency-following responses (FFRs) were recorded from unanesthetized cats with electrodes chronically implanted in the cochlear nucleus and on the round window. Tone bursts of different frequencies (irrelevant stimuli) were presented repetitively (85 dB SPL, 1/sec) as background before, during, and after the presentation of a visual discrimination task (relevant stimuli) which attempted to alter the attentive state of the animals. The mean peak-to-peak amplitudes of the FFRs from the cochlear nucleus were significantly reduced in amplitude during attention to the visual discrimination stimuli when compared with the amplitudes of the pretest- and posttest-control periods. However, at the round window (cochlear microphonic) no significant differences in amplitude were observed for the same periods. Although the amplitudes of the FFRs were reduced in amplitude at all frequencies during visual attention, much greater suppression occurred at the middle frequencies (700-2000 Hz) than at higher or lower frequencies. These data suggest that during visual attention the FFRs are attenuated by a central inhibitory mechanism.
The cochlear microphonic response to continuous pure tones has been recorded in the 'far field' from the scalps of anesthetized cats. Previous methods for scalp recording used tone pip transients only. Our experiments show that the observed wave forms are not due to electrical or mechanoelectrical artifacts. Neural responses such as brain stem responses or the frequency-following response have been excluded as major contributors to the observed wave forms, which are virtually identical to the round window cochlear microphonic response with respect to (1) wave shape with non-sinusoidal stimuli, (2) intensity-amplitude functions, (3) response phase, and (4) amplitude changes due to superimposed band-limited white noise. The methods of ruling out significant artifacts are applicable to non-invasive recordings from humans.
The responses from the round window of the cochlea and the surface of the cochlear nucleus to continuous tones and noise that were amplitude-modulated with pseudorandom noise were studied. The responses were averaged with the averager locked to the periodicity of the pseudorandom noise, and the cross-correlation between the averaged responses and one period of the pseudorandom noise was computed. The degrees of non-linearities in the responses were estimated by comparing the response of a linear model that had this cross-correlogram as its impulse response and the physiological response. The root mean square (RMS) value of the histograms increases as a function of the stimulus intensity and reaches a peak at 40-60 dB above threshold, above which intensity it decreases. The non-linear component of the response increases monotonically with sound intensity in the range from threshold to 60-70 dB above threshold. The pseudorandom noise was of the inverse-repeat type, and when even-order non-linearities were canceled by subtracting the latter half of the responses to one period of the pseudorandom noise from the first half a much closer agreement with the model responses was obtained, indicating that the non-linearities were mainly of even order. It was concluded that the non-linearities of the responses may have been caused by an unequal response to increases and decreases in stimulus intensity.
Short-latency potentials evoked by round window electrical stimulation were recorded in guinea pig by means of vertex-pinna skin electrodes using averaging techniques. Constant current shocks of 20 microseconds or 50 microseconds (25-300 microA) were used to evoke both auditory and vestibular brain-stem potentials. Pure auditory potentials, comparable to those evoked by acoustic clicks, were obtained by 20 microseconds electrical stimuli and disappeared during an auditory masking procedure made with a continuous white noise (110 dB SPL). Short latency potentials labeled V1, V2 and V3 were obtained by 50 microseconds electrical stimuli during an auditory masking procedure. This response disappeared after specific vestibular neurectomy, whereas the auditory response evoked by acoustic clicks or by electrical stimulation remained unchanged, suggesting that these latter potentials had a vestibular origin.